Malcolm R D, Alkana R L
Pharmacol Biochem Behav. 1982 Feb;16(2):341-6. doi: 10.1016/0091-3057(82)90169-1.
Three studies investigated the mechanism of hyperbaric ethanol antagonism. C57 Bl/6j mice were injected intraperitoneally with 3.6 g/kg ethanol and were exposed to 1-12 atmospheres absolute (ATA) helium-oxygen or to 1 ATA air at temperatures that offset the cooling effects of helium or helium and ethanol. Hyperbaric treatment significantly reduced sleep-time and increased wake-up brain ethanol concentrations compared to temperature matched controls. Treatment with 12 ATA helium-oxygen increased the brain ethanol concentration and the brain-blood ethanol ratio at 150 minutes after ethanol administration. These results exclude helium or pressure-induced changes in body temperature, rate of blood ethanol decline or distribution to the brain as mechanisms mediating the antagonism. The data support a membrane site of antagonism.
三项研究对高压乙醇拮抗作用的机制进行了调查。给C57 Bl/6j小鼠腹腔注射3.6克/千克乙醇,并将其置于1至12绝对大气压(ATA)的氦氧环境中,或在抵消氦气或氦气与乙醇冷却效应的温度下置于1 ATA空气环境中。与温度匹配的对照组相比,高压治疗显著缩短了睡眠时间,并提高了清醒时大脑中的乙醇浓度。用12 ATA氦氧治疗在乙醇给药后150分钟时提高了大脑乙醇浓度和脑血乙醇比率。这些结果排除了氦气或压力引起的体温变化、血液乙醇下降速率或向大脑分布作为介导拮抗作用的机制。数据支持拮抗作用的膜位点。